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000827653 0247_ $$2doi$$a10.1016/j.biopsych.2016.06.008
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000827653 1001_ $$0P:(DE-HGF)0$$aSchoch, Hannah$$b0
000827653 245__ $$aSociability Deficits and Altered Amygdala Circuits in Mice Lacking Pcdh10, an Autism Associated Gene
000827653 260__ $$aAmsterdam [u.a.]$$bElsevier Science$$c2017
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000827653 520__ $$aBackgroundBehavioral symptoms in individuals with autism spectrum disorder (ASD) have been attributed to abnormal neuronal connectivity, but the molecular bases of these behavioral and brain phenotypes are largely unknown. Human genetic studies have implicated PCDH10, a member of the δ2 subfamily of nonclustered protocadherin genes, in ASD. PCDH10 expression is enriched in the basolateral amygdala, a brain region implicated in the social deficits of ASD. Previous reports indicate that Pcdh10 plays a role in axon outgrowth and glutamatergic synapse elimination, but its roles in social behaviors and amygdala neuronal connectivity are unknown. We hypothesized that haploinsufficiency of Pcdh10 would reduce social approach behavior and alter the structure and function of amygdala circuits.MethodsMice lacking one copy of Pcdh10 (Pcdh10+/–) and wild-type littermates were assessed for social approach and other behaviors. The lateral/basolateral amygdala was assessed for dendritic spine number and morphology, and amygdala circuit function was studied using voltage-sensitive dye imaging. Expression of Pcdh10 and N-methyl-D-aspartate receptor (NMDAR) subunits was assessed in postsynaptic density fractions of the amygdala.ResultsMale Pcdh10+/– mice have reduced social approach behavior, as well as impaired gamma synchronization, abnormal spine morphology, and reduced levels of NMDAR subunits in the amygdala. Social approach deficits in Pcdh10+/– male mice were rescued with acute treatment with the NMDAR partial agonist d-cycloserine.ConclusionsOur studies reveal that male Pcdh10+/– mice have synaptic and behavioral deficits, and establish Pcdh10+/– mice as a novel genetic model for investigating neural circuitry and behavioral changes relevant to ASD.
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000827653 7001_ $$0P:(DE-HGF)0$$aKreibich, Arati S.$$b1
000827653 7001_ $$0P:(DE-HGF)0$$aFerri, Sarah L.$$b2
000827653 7001_ $$0P:(DE-HGF)0$$aWhite, Rachel S.$$b3
000827653 7001_ $$0P:(DE-HGF)0$$aBohorquez, Dominique$$b4
000827653 7001_ $$0P:(DE-HGF)0$$aBanerjee, Anamika$$b5
000827653 7001_ $$0P:(DE-HGF)0$$aPort, Russell G.$$b6
000827653 7001_ $$0P:(DE-HGF)0$$aDow, Holly C.$$b7
000827653 7001_ $$0P:(DE-HGF)0$$aCordero, Lucero$$b8
000827653 7001_ $$0P:(DE-HGF)0$$aPallathra, Ashley A.$$b9
000827653 7001_ $$0P:(DE-HGF)0$$aKim, Hyong$$b10
000827653 7001_ $$0P:(DE-HGF)0$$aLi, Hongzhe$$b11
000827653 7001_ $$0P:(DE-HGF)0$$aBilker, Warren B.$$b12
000827653 7001_ $$0P:(DE-HGF)0$$aHirano, Shinji$$b13
000827653 7001_ $$0P:(DE-HGF)0$$aSchultz, Robert T.$$b14
000827653 7001_ $$0P:(DE-HGF)0$$aBorgmann-Winter, Karin$$b15
000827653 7001_ $$0P:(DE-HGF)0$$aHahn, Chang-Gyu$$b16
000827653 7001_ $$0P:(DE-Juel1)131680$$aFeldmeyer, Dirk$$b17
000827653 7001_ $$0P:(DE-HGF)0$$aCarlson, Gregory C.$$b18
000827653 7001_ $$0P:(DE-HGF)0$$aAbel, Ted$$b19
000827653 7001_ $$0P:(DE-HGF)0$$aBrodkin, Edward S.$$b20$$eCorresponding author
000827653 773__ $$0PERI:(DE-600)1499907-9$$a10.1016/j.biopsych.2016.06.008$$gVol. 81, no. 3, p. 193 - 202$$n3$$p193 - 202$$tBiological psychiatry$$v81$$x0006-3223$$y2017
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